The efforts detailed within are steps in the overall goal of utilizing intracellular indicators of oxidative metabolic activity to assess the changes that occur during cerebral anoxia/ischemia and to determine the factors most critical to overall tissue viability during and following periods of circulatory compromise. Non-invasive techniques of fluorometrically monitoring changes in the reduction/oxidation ratio of intramitochondrial NAD and the technique of reflection spectrophotometry to measure redox changes of cytochromes together with changes in hemoglobin oxygenation and local blood volume will be utilized. The new procedure of "rapid-scanning fluorospectrophotometry" will be employed to monitor simultaneously all of these parameters in intact CNS tissues. The advantage of these procedures is that they require no invasive assay sampling and allow the tissue to remain intact, normally or abnormally circulated with cellular, anatomical and physiological relationships intact. Simultaneous to detection by these optical procedures, parameters of electrophysiological function such as shifts of steady potential, ECoG, evoked potential activity and extracellular potassium will be recorded from the same tissue area. By relating parameters of metabolism and function, we will discern how vulnerability of functional activity is associated with periods of ischemic insult. We will continue efforts to define the relationships between energy metabolism and CNS functioning to increase our understanding of how and why the brain utilized oxygen, metabolic substrates and oxidative energy and to determine how viability is threatened by the loss of oxygen and circulatory perfusion.